A muscle fiber can only get so big with one myonuclei. In order to undergo further hypertrophy more myonuclei must be added and they come from the proliferation of satellite cells that get incorporated into existing fibers. If you irradiate a rat hindlimb, you prevent the SC from proliferating, subject the rat to any sort of hypertrophy model and the limb that was irradiated will not hypertrophy, the other will. I won't get into hyperplasia bc that's still a mystery if it really exists, but hypertrophy has a well established mechanism and involves a number of variables but SC are critical to the process. In the end, the more you have per unit muscle CSA (cross sectional area), the greater the hypertrophy potential. The East Germans knew this decades ago. They could juice a female track and field athlete long before they would be drug tested and with solid training and dietary intake, maintain a good portion of what was gained during her cycle and test clean. Bottom line, once juiced, always juiced and chromosomes aside this is why simply reducing T in a trans female does not equal the playing field against cis women, likewise once juiced, never a natty again, male or female in any playing field. The other question is which AAS does what. The androgen receptor is the primary mechanism but many of these drugs may have other non-genomic pathways to hypertrophy beyond the AR.
